Base de dados : MEDLINE
Pesquisa : D12.776.157.170.250 [Categoria DeCS]
Referências encontradas : 1400 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 140 ir para página                         

  1 / 1400 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28985842
[Au] Autor:Tani G; Tomuschat C; O'Donnell AM; Coyle D; Puri P
[Ad] Endereço:National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin, Ireland.
[Ti] Título:Increased population of immature enteric glial cells in the resected proximal ganglionic bowel of Hirschsprung's disease patients.
[So] Source:J Surg Res;218:150-155, 2017 Oct.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Enteric glial cells are essential for normal gastrointestinal function. Abnormalities in glial structure, development, or function lead to disturbances in gastrointestinal physiology. Fatty acid-binding protein 7 (FABP7) is a marker of immature enteric glial cells, whereas S100 is expressed only by mature glial cells. Patients with Hirschsprung's disease (HSCR) often suffer from dysmotility and enterocolitis despite proper surgery. We designed this study to determine the distribution and expression of glial cells in patients with HSCR compared to normal controls. METHODS: We investigated FABP7, S100, and PGP 9.5 expressions in both the ganglionic and aganglionic bowel of patients with HSCR (n = 6) versus normal control colon (n = 6). Protein distribution was assessed by using immunofluorescence and confocal microscopy. Gene and protein expressions were quantified using quantitative real-time polymerase chain reaction (qPCR), Western blot analysis, and densitometry. RESULTS: qPCR and Western blot analysis demonstrated a significantly increased FABP7 expression in ganglionic specimens compared to control specimen (P < 0.05). Confocal microscopy revealed FABP7 glia cells lie under the colonic epithelium and in close apposition to enteric neurons in the ganglionic bowel. CONCLUSIONS: The significantly increased number of immature enteric glial cells (EGCs) in the ganglionic bowel of HSCR patients may have adverse effect on the function of enteric neurons and intestinal barrier and thus predispose these patients to intestinal motility problems and enterocolitis.
[Mh] Termos MeSH primário: Doença de Hirschsprung/patologia
Plexo Mientérico/patologia
Neuroglia/patologia
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Estudos de Casos e Controles
Proteína 7 de Ligação a Ácidos Graxos/metabolismo
Seres Humanos
Plexo Mientérico/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


  2 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28844908
[Au] Autor:Laprairie RB; Denovan-Wright EM; Wright JM
[Ad] Endereço:Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada. Electronic address: robert.laprairie@dal.ca.
[Ti] Título:Differential regulation of the duplicated fabp7, fabp10 and fabp11 genes of zebrafish by peroxisome proliferator activated receptors.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;213:81-90, 2017 Nov.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the duplication-degeneration-complementation model, duplicated gene-pairs undergo nonfunctionalization (loss from the genome), subfunctionalization (the functions of the ancestral gene are sub-divided between duplicate genes), or neofunctionalization (one of the duplicate genes acquires a new function). These processes occur by loss or gain of regulatory elements in gene promoters. Fatty acid-binding proteins (Fabp) belong to a multigene family composed of orthologous proteins that are highly conserved in sequence and function, but differ in their gene regulation. We previously reported that the zebrafish fabp1a, fabp1b.1, and fabp1b.2 promoters underwent subfunctionalization of PPAR responsiveness. Here, we describe the regulation at the duplicated zebrafish fabp7a/fabp7b, fabp10a/fabp10b and fabp11a/fabp11b gene promoters. Differential control at the duplicated fabp promoters was assessed by DNA sequence analysis, responsiveness to PPAR-isoform specific agonists and NF-κB p50 antagonists in zebrafish liver and intestine explant tissue, and in HEK293A cells transfected with fabp promoter-reporter constructs. Each zebrafish fabp gene displayed unique transcriptional regulation compared to its paralogous duplicate. This work provides a framework to account for the evolutionary trajectories that led to the high retention (57%) of duplicated fabp genes in the zebrafish genome compared to only ~3% of all duplicated genes in the zebrafish genome.
[Mh] Termos MeSH primário: Proteína 7 de Ligação a Ácidos Graxos/biossíntese
Proteínas de Ligação a Ácido Graxo/biossíntese
Duplicação Gênica
Regulação da Expressão Gênica/fisiologia
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Proteínas de Peixe-Zebra/biossíntese
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína 7 de Ligação a Ácidos Graxos/genética
Proteínas de Ligação a Ácido Graxo/genética
Células HEK293
Seres Humanos
Subunidade p50 de NF-kappa B/genética
Subunidade p50 de NF-kappa B/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/genética
Regiões Promotoras Genéticas/fisiologia
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fabp11 protein, zebrafish); 0 (Fatty Acid-Binding Protein 7); 0 (Fatty Acid-Binding Proteins); 0 (NF-kappa B p50 Subunit); 0 (NFKB1 protein, human); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Zebrafish Proteins); 0 (fabp7a protein, zebrafish); 0 (fatty acid-binding protein 10, zebrafish)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


  3 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28816095
[Au] Autor:Halford J; Shen S; Itamura K; Levine J; Chong AC; Czerwieniec G; Glenn TC; Hovda DA; Vespa P; Bullock R; Dietrich WD; Mondello S; Loo JA; Wanner IB
[Ad] Endereço:1 Semel Institute for Neuroscience and Human Behavior, 12222 University of California , Los Angeles, CA, USA.
[Ti] Título:New astroglial injury-defined biomarkers for neurotrauma assessment.
[So] Source:J Cereb Blood Flow Metab;37(10):3278-3299, 2017 Oct.
[Is] ISSN:1559-7016
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traumatic brain injury (TBI) is an expanding public health epidemic with pathophysiology that is difficult to diagnose and thus treat. TBI biomarkers should assess patients across severities and reveal pathophysiology, but currently, their kinetics and specificity are unclear. No single ideal TBI biomarker exists. We identified new candidates from a TBI CSF proteome by selecting trauma-released, astrocyte-enriched proteins including aldolase C (ALDOC), its 38kD breakdown product (BDP), brain lipid binding protein (BLBP), astrocytic phosphoprotein (PEA15), glutamine synthetase (GS) and new 18-25kD-GFAP-BDPs. Their levels increased over four orders of magnitude in severe TBI CSF. First post-injury week, ALDOC levels were markedly high and stable. Short-lived BLBP and PEA15 related to injury progression. ALDOC, BLBP and PEA15 appeared hyper-acutely and were similarly robust in severe and mild TBI blood; 25kD-GFAP-BDP appeared overnight after TBI and was rarely present after mild TBI. Using a human culture trauma model, we investigated biomarker kinetics. Wounded (mechanoporated) astrocytes released ALDOC, BLBP and PEA15 acutely. Delayed cell death corresponded with GFAP release and proteolysis into small GFAP-BDPs. Associating biomarkers with cellular injury stages produced astroglial injury-defined (AID) biomarkers that facilitate TBI assessment, as neurological deficits are rooted not only in death of CNS cells, but also in their functional compromise.
[Mh] Termos MeSH primário: Astrócitos/patologia
Biomarcadores/análise
Lesões Encefálicas Traumáticas/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Astrócitos/química
Concussão Encefálica
Lesões Encefálicas Traumáticas/diagnóstico
Células Cultivadas
Proteína 7 de Ligação a Ácidos Graxos/sangue
Frutose-Bifosfato Aldolase/sangue
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/sangue
Cinética
Fosfoproteínas/sangue
Proteoma/análise
Proteínas Supressoras de Tumor/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Intracellular Signaling Peptides and Proteins); 0 (PEA15 protein, human); 0 (Phosphoproteins); 0 (Proteome); 0 (Tumor Suppressor Proteins); EC 4.1.2.13 (Fructose-Bisphosphate Aldolase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1177/0271678X17724681


  4 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28632393
[Au] Autor:Hsu HC; Tong S; Zhou Y; Elmes MW; Yan S; Kaczocha M; Deutsch DG; Rizzo RC; Ojima I; Li H
[Ad] Endereço:Cryo-EM Structural Biology Laboratory, Van Andel Research Institute , Grand Rapids, Michigan 49503, United States.
[Ti] Título:The Antinociceptive Agent SBFI-26 Binds to Anandamide Transporters FABP5 and FABP7 at Two Different Sites.
[So] Source:Biochemistry;56(27):3454-3462, 2017 Jul 11.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human FABP5 and FABP7 are intracellular endocannabinoid transporters. SBFI-26 is an α-truxillic acid 1-naphthyl monoester that competitively inhibits the activities of FABP5 and FABP7 and produces antinociceptive and anti-inflammatory effects in mice. The synthesis of SBFI-26 yields several stereoisomers, and it is not known how the inhibitor binds the transporters. Here we report co-crystal structures of SBFI-26 in complex with human FABP5 and FABP7 at 2.2 and 1.9 Å resolution, respectively. We found that only (S)-SBFI-26 was present in the crystal structures. The inhibitor largely mimics the fatty acid binding pattern, but it also has several unique interactions. Notably, the FABP7 complex corroborates key aspects of the ligand binding pose at the canonical site previously predicted by virtual screening. In FABP5, SBFI-26 was unexpectedly found to bind at the substrate entry portal region in addition to binding at the canonical ligand-binding pocket. Our structural and binding energy analyses indicate that both R and S forms appear to bind the transporter equally well. We suggest that the S enantiomer observed in the crystal structures may be a result of the crystallization process selectively incorporating the (S)-SBFI-26-FABP complexes into the growing lattice, or that the S enantiomer may bind to the portal site more rapidly than to the canonical site, leading to an increased local concentration of the S enantiomer for binding to the canonical site. Our work reveals two binding poses of SBFI-26 in its target transporters. This knowledge will guide the development of more potent FABP inhibitors based upon the SBFI-26 scaffold.
[Mh] Termos MeSH primário: Analgésicos/metabolismo
Ciclobutanos/metabolismo
Ácidos Dicarboxílicos/metabolismo
Proteína 7 de Ligação a Ácidos Graxos/metabolismo
Proteínas de Ligação a Ácido Graxo/metabolismo
Modelos Moleculares
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Analgésicos/química
Analgésicos/farmacologia
Animais
Anti-Inflamatórios não Esteroides/química
Anti-Inflamatórios não Esteroides/metabolismo
Anti-Inflamatórios não Esteroides/farmacologia
Apoproteínas/antagonistas & inibidores
Apoproteínas/química
Apoproteínas/genética
Apoproteínas/metabolismo
Sítios de Ligação
Domínio Catalítico
Biologia Computacional
Cristalografia por Raios X
Ciclobutanos/química
Ciclobutanos/farmacologia
Ácidos Dicarboxílicos/química
Ácidos Dicarboxílicos/farmacologia
Proteína 7 de Ligação a Ácidos Graxos/antagonistas & inibidores
Proteína 7 de Ligação a Ácidos Graxos/química
Proteína 7 de Ligação a Ácidos Graxos/genética
Proteínas de Ligação a Ácido Graxo/antagonistas & inibidores
Proteínas de Ligação a Ácido Graxo/química
Proteínas de Ligação a Ácido Graxo/genética
Seres Humanos
Ligantes
Camundongos
Conformação Molecular
Simulação de Acoplamento Molecular
Simulação de Dinâmica Molecular
Conformação Proteica
Proteínas Recombinantes
Estereoisomerismo
Proteínas Supressoras de Tumor/antagonistas & inibidores
Proteínas Supressoras de Tumor/química
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-naphthyl alpha-truxillate); 0 (Analgesics); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Apoproteins); 0 (Cyclobutanes); 0 (Dicarboxylic Acids); 0 (FABP5 protein, human); 0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Fatty Acid-Binding Proteins); 0 (Ligands); 0 (Recombinant Proteins); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00194


  5 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28578832
[Au] Autor:Petecchia L; Viti F; Sbrana F; Vassalli M; Gavazzo P
[Ad] Endereço:Institute of Biophysics, National Research Council, Via De Marini 6, 16149 Genova, Italy.
[Ti] Título:A biophysical approach to quantify skeletal stem cells trans-differentiation as a model for the study of osteoporosis.
[So] Source:Biophys Chem;229:84-92, 2017 Oct.
[Is] ISSN:1873-4200
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The stroma of human bone marrow contains a population of skeletal stem cells (hBM-MSC) which are common ancestors, among the others, of osteoblasts and adipocytes. It has been proposed that the imbalance between hBM-MSC osteogenesis and adipogenesis, which naturally accompanies bone marrow senescence, may contribute to the development of bone-associated diseases, like osteoporosis. The possibility to reproduce this mechanism in vitro has been demonstrated, providing a good model to disclose the details of the complex bone-fat generation homeostasis. Nevertheless, the lack of a simple approach to quantitatively assess the actual stage of a cellular population hindered the adoption of this in vitro model. In this work, the direct differentiation of hBM-MSCs towards a single (osteo or adipo) lineage was characterized using quantitative biophysical and biological approaches, together with the parallel process of trans-differentiation from one lineage to the other. The results confirm that the original plasticity of hBM-MSCs is maintained along the initial stages of the differentiation, showing that in vitro conversion of pre-osteoblasts into adipocytes and, vice versa, of pre-adipocytes into osteoblasts is extremely efficient, comparable with the direct differentiation. Moreover, a method based on digital holography is proposed, providing a quantitative indication of the phenotype stage along differentiation.
[Mh] Termos MeSH primário: Transdiferenciação Celular
Células Mesenquimais Estromais/citologia
Modelos Biológicos
Osteoporose/fisiopatologia
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/metabolismo
Fenômenos Biofísicos
Células da Medula Óssea/citologia
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Proteína 7 de Ligação a Ácidos Graxos/genética
Proteína 7 de Ligação a Ácidos Graxos/metabolismo
Holografia
Seres Humanos
Imagem Tridimensional
Células Mesenquimais Estromais/metabolismo
Microscopia de Contraste de Fase
Osteoblastos/citologia
Osteoblastos/metabolismo
Osteocalcina/genética
Osteocalcina/metabolismo
Osteoporose/metabolismo
RNA/isolamento & purificação
RNA/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Tumor Suppressor Proteins); 104982-03-8 (Osteocalcin); 63231-63-0 (RNA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


  6 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27787894
[Au] Autor:Tripathi S; Kushwaha R; Mishra J; Gupta MK; Kumar H; Sanyal S; Singh D; Sanyal S; Sahasrabuddhe AA; Kamthan M; Mudiam MK; Bandyopadhyay S
[Ad] Endereço:Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (IITR), Lucknow, India.
[Ti] Título:Docosahexaenoic acid up-regulates both PI3K/AKT-dependent FABP7-PPARγ interaction and MKP3 that enhance GFAP in developing rat brain astrocytes.
[So] Source:J Neurochem;140(1):96-113, 2017 Jan.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The astrocyte marker, glial fibrillary acidic protein (GFAP), has essential functions in the brain, but may trigger astroglial scarring when expressed in excess. Docosahexaenoic acid (DHA) is an n-3 fatty acid that is protective during brain development. However, the effect of DHA on GFAP levels of developing brain remains unexplored. Here, we detected that treating developing rats with DHA-enriched fish-oil caused dose-dependent GFAP augmentation. We investigated the mechanism promoting GFAP, hypothesizing the participation of fatty acid-binding protein-7 (FABP7), known to bind DHA. We identified that DHA stimulated FABP7 expression in astrocytes, and FABP7-silencing suppressed DHA-induced GFAP, indicating FABP7-mediated GFAP increase. Further investigation proved FABP7 expression to be phosphatidylinositide 3-kinases (PI3K)/AKT and nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARγ)-dependent. We found that PI3K/AKT activated PPARγ that triggered FABP7 expression via PPARγ-responsive elements within its gene. Towards identifying FABP7-downstream pathways, we considered our previous report that demonstrated cyclin-dependent kinase-5 (CDK5)-PPARγ-protein-protein complex to suppress GFAP. We found that the DHA-induced FABP7 underwent protein-protein interaction with PPARγ, which impeded CDK5-PPARγ formation. Hence, it appeared that enhanced FABP7-PPARγ in lieu of CDK5-PPARγ resulted in increased GFAP. PI3K/AKT not only stimulated formation of FABP7-PPARγ protein-protein complex, but also up-regulated a FABP7-independent MAP-kinase-phosphatase-3 pathway that inactivated CDK5 and hence attenuated CDK5-PPARγ. Overall, our data reveal that via the proximal PI3K/AKT, DHA induces FABP7-PPARγ, through genomic and non-genomic mechanisms, and MAP-kinase-phosphatase-3 that converged at attenuated CDK5-PPARγ and therefore, enhanced GFAP. Accordingly, our study demonstrates a DHA-mediated astroglial hyperactivation, pointing toward a probable injurious role of DHA in brain development.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Ácidos Docosa-Hexaenoicos/farmacologia
Fosfatase 6 de Especificidade Dupla/biossíntese
Proteína 7 de Ligação a Ácidos Graxos/biossíntese
Proteína Glial Fibrilar Ácida/biossíntese
Proteína Oncogênica v-akt/biossíntese
PPAR gama/biossíntese
[Mh] Termos MeSH secundário: Animais
Astrócitos/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Encéfalo/crescimento & desenvolvimento
Encéfalo/metabolismo
Células Cultivadas
Relação Dose-Resposta a Droga
Feminino
Masculino
Ligação Proteica/fisiologia
Ratos
Ratos Wistar
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fabp7 protein, rat); 0 (Fatty Acid-Binding Protein 7); 0 (Glial Fibrillary Acidic Protein); 0 (PPAR gamma); 0 (glial fibrillary acid protein, rat); 25167-62-8 (Docosahexaenoic Acids); EC 2.7.11.1 (Oncogene Protein v-akt); EC 3.1.3.48 (Dual Specificity Phosphatase 6)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13879


  7 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27126899
[Au] Autor:Ilzecki M; Ilzecka J; Przywara S; Terlecki P; Grabarska A; Stepulak A; Zubilewicz T
[Ad] Endereço:Chair and Department of Vascular Surgery and Angiology, Medical University of Lublin, Lublin, Poland.
[Ti] Título:Effect of carotid endarterectomy on brain damage markers.
[So] Source:Acta Neurol Scand;135(3):352-359, 2017 Mar.
[Is] ISSN:1600-0404
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Carotid endarterectomy (CEA) is a recommended treatment in the prevention of ischemic stroke. However, this procedure may cause neurological complications caused by cerebrovascular damage. While YKL-40 is a proinflammatory protein, neurofilament light polypeptide (NEFL) and brain lipid-binding protein (FABP7) are structural components of the brain. The aim of the study was to investigate YKL-40, NEFL, and FABP7 in the serum of patients undergoing CEA. MATERIALS AND METHODS: The study included 25 participants who underwent CEA due to internal carotid artery stenosis. Blood samples were taken from each patient at three different intervals: prior to the surgery, 12 h after the surgery, and 48 h after the surgery. Serum levels of these brain damage markers were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The study showed that the serum YKL-40 level was significantly increased 48 h after CEA when compared to the level prior to surgery and also when compared to levels 12 h after surgery. There were no statistically significant differences in serum NEFL and FABP7 levels between all three recorded measurements. CONCLUSIONS: Data from our study showed that CEA affects serum YKL-40 but not NEFL and FABP7 levels. This implicates that YKL-40 may be a valuable serum marker of brain damage after CEA. However, the observed change in serum YKL-40 level in patients after CEA does not necessarily warrant a change in recommendations concerning the use of this treatment in patients with high-grade internal carotid artery stenosis.
[Mh] Termos MeSH primário: Estenose das Carótidas/cirurgia
Proteína 1 Semelhante à Quitinase-3/sangue
Endarterectomia das Carótidas/efeitos adversos
Proteína 7 de Ligação a Ácidos Graxos/sangue
Proteínas de Neurofilamentos/sangue
Complicações Pós-Operatórias/sangue
Acidente Vascular Cerebral/prevenção & controle
Proteínas Supressoras de Tumor/sangue
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CHI3L1 protein, human); 0 (Chitinase-3-Like Protein 1); 0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Neurofilament Proteins); 0 (Tumor Suppressor Proteins); 0 (neurofilament protein L)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160430
[St] Status:MEDLINE
[do] DOI:10.1111/ane.12607


  8 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27817785
[Au] Autor:Li XW; Li F; Liu J; Wang Y; Fu W
[Ad] Endereço:Department of Neonatology, Rocket Army General Hospital of the Chinese People's Liberation Army, Jinzhou Medical University, Beijing 100700, China. liujingbj@sina.com.
[Ti] Título:[Effect of antepartum taurine supplementation in regulating the activity of Rho family factors and promoting the proliferation of neural stem cells in neonatal rats with fetal growth restriction].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;18(11):1158-1165, 2016 Nov.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To study the possible effect of antepartum taurine supplementation in regulating the activity of Rho family factors and promoting the proliferation of neural stem cells in neonatal rats with fetal growth restriction (FGR), and to provide a basis for antepartum taurine supplementation to promote brain development in children with FGR. METHODS: A total of 24 pregnant Sprague-Dawley rats were randomly divided into three groups: control, FGR, and taurine (n=8 each ). A rat model of FGR was established by food restriction throughout pregnancy. RT-PCR, immunohistochemistry, and Western blot were used to measure the expression of the specific intracellular markers for neural stem cells fatty acid binding protein 7 (FABP7), Rho-associated coiled-coil containing protein kinase 2 (ROCK2), ras homolog gene family, member A (RhoA), and Ras-related C3 botulinum toxin substrate (Rac). RESULTS: The FGR group had significantly lower OD value of FABP7-positive cells and mRNA and protein expression of FABP7 than the control group, and the taurine group had significantly higher OD value of FABP7-positive cells and mRNA and protein expression of FABP7 than the FGR group (P<0.05). The FGR group had significantly higher mRNA expression of RhoA and ROCK2 than the control group. The taurine group had significantly higher mRNA expression of RhoA and ROCK2 than the control group and significantly lower expression than the FGR group (P<0.05). The FGR group had significantly lower mRNA expression of Rac than the control group. The taurine group had significantly higher mRNA expression of Rac than the FGR and control groups (P<0.05). The FGR group had significantly higher protein expression of RhoA and ROCK2 than the control group. The taurine group had significantly lower protein expression of RhoA and ROCK2 than the FGR group (P<0.05). CONCLUSIONS: Antepartum taurine supplementation can promote the proliferation of neural stem cells in rats with FGR, and its mechanism may be related to the regulation of the activity of Rho family factors.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Retardo do Crescimento Fetal/tratamento farmacológico
Células-Tronco Neurais/efeitos dos fármacos
Taurina/farmacologia
Quinases Associadas a rho/genética
Proteína rhoA de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Peso Corporal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Proteína 7 de Ligação a Ácidos Graxos/análise
Feminino
Masculino
Células-Tronco Neurais/fisiologia
Ratos
Ratos Sprague-Dawley
Quinases Associadas a rho/análise
Proteína rhoA de Ligação ao GTP/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fabp7 protein, rat); 0 (Fatty Acid-Binding Protein 7); 1EQV5MLY3D (Taurine); EC 2.7.11.1 (ROCK2 protein, rat); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


  9 / 1400 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27367508
[Au] Autor:Su X; Tan QS; Parikh BH; Tan A; Mehta MN; Sia Wey Y; Tun SB; Li LJ; Han XY; Wong TY; Hunziker W; Luu CD; Owada Y; Barathi VA; Zhang SS; Chaurasia SS
[Ad] Endereço:Singapore Eye Research Institute Singapore National Eye Centre, Singapore 2Institute of Molecular Cell Biology, SIPRAD (IMCB-SERI Program in Retinal Angiogenic Diseases), A*STAR, Singapore 3Department of Ophthalmology, Yong Loo Lin School of Medicine, Nat.
[Ti] Título:Characterization of Fatty Acid Binding Protein 7 (FABP7) in the Murine Retina.
[So] Source:Invest Ophthalmol Vis Sci;57(7):3397-408, 2016 06 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To characterize the mouse retina lacking fatty acid binding protein (FABP7-/-). METHODS: Immunohistochemistry (IHC) was performed in 8-week-old mice to localize FABP7 in the retina. Retinal thickness was measured using image-guided spectral-domain optical coherence topography images. Electroretinography was carried out to assess retinal function. Fundus photography and fundus fluorescein angiography were performed on FABP7-/- and littermate wild-type (WT) mice, and retinal vascular changes were calculated using Singapore I Vessel Assessment (SIVA) analysis. Blood glucose levels were measured in the 8-week-old WT and FABP7-/- mice. In addition, retina was processed for trypsin digestion and retinal flat mounts for isolectin staining. Transcript levels of FABP7, VEGF, GFAP, and Na+K+ATPase were quantified using real-time PCR, and protein expression was analyzed by IHC and Western blot. RESULTS: Fatty acid binding protein 7 is expressed in the inner nuclear layer, outer plexiform layer, and photoreceptor inner segments. No significant difference in retinal thickness and ERG responses was observed between FABP7-deficient and WT retinas. FABP7-/- mice have significantly decreased retinal venular caliber retinal arteriolar fractal dimension compared with WT littermates. FABP7-/- mice showed significant increased areas of fluorescein leakage in the retina. FABP7-/- mice exhibited elevated high blood glucose levels compared with WT mice. Trypsin digested FABP7-/- mice retina showed increased acellular strands and endothelial cell drop outs, and reduced microvasculature branching compared with WT retina. FABP7-/- mice retina also have increased GFAP and VEGF expression. CONCLUSIONS: Fatty acid binding protein 7 is expressed in the retina and might play an important role in maintaining retinal vasculature.
[Mh] Termos MeSH primário: Proteína 7 de Ligação a Ácidos Graxos/metabolismo
Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia/análise
Western Blotting
Modelos Animais de Doenças
Eletrorretinografia
Proteína 7 de Ligação a Ácidos Graxos/deficiência
Angiofluoresceinografia
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Retina/fisiopatologia
Degeneração Retiniana/metabolismo
Degeneração Retiniana/fisiopatologia
Vasos Retinianos/fisiopatologia
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Fatty Acid-Binding Protein 7)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.15-18542


  10 / 1400 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27084744
[Au] Autor:Panaccione A; Chang MT; Carbone BE; Guo Y; Moskaluk CA; Virk RK; Chiriboga L; Prasad ML; Judson B; Mehra S; Yarbrough WG; Ivanov SV
[Ad] Endereço:Department of Surgery, Section of Otolaryngology, Yale School of Medicine, New Haven, Connecticut. Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee.
[Ti] Título:NOTCH1 and SOX10 are Essential for Proliferation and Radiation Resistance of Cancer Stem-Like Cells in Adenoid Cystic Carcinoma.
[So] Source:Clin Cancer Res;22(8):2083-95, 2016 Apr 15.
[Is] ISSN:1078-0432
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Although the existence of cancer stem cells (CSC) in adenoid cystic carcinoma (ACC) has been proposed, lack of assays for their propagation and uncertainty about molecular markers prevented their characterization. Our objective was to isolate CSC from ACC and provide insight into signaling pathways that support their propagation. EXPERIMENTAL DESIGN: To isolate CSC from ACC and characterize them, we used ROCK inhibitor-supplemented cell culture, immunomagnetic cell sorting, andin vitro/in vivoassays for CSC viability and tumorigenicity. RESULTS: We identified in ACC CD133-positive CSC that expressed NOTCH1 and SOX10, formed spheroids, and initiated tumors in nude mice. CD133(+)ACC cells produced activated NOTCH1 (N1ICD) and generated CD133(-)cells that expressed JAG1 as well as neural differentiation factors NR2F1, NR2F2, and p27Kip1. Knockdowns ofNOTCH1, SOX10, and their common effectorFABP7had negative effects on each other, inhibited spheroidogenesis, and induced cell death pointing at their essential roles in CSC maintenance. Downstream effects ofFABP7knockdown included suppression of a broad spectrum of genes involved in proliferation, ribosome biogenesis, and metabolism. Among proliferation-linked NOTCH1/FABP7 targets, we identified SKP2 and its substrate p27Kip1. A γ-secretase inhibitor, DAPT, selectively depleted CD133(+)cells, suppressed N1ICD and SKP2, induced p27Kip1, inhibited ACC growthin vivo, and sensitized CD133(+)cells to radiation. CONCLUSIONS: These results establish in the majority of ACC the presence of a previously uncharacterized population of CD133(+)cells with neural stem properties, which are driven by SOX10, NOTCH1, and FABP7. Sensitivity of these cells to Notch inhibition and their dependence on SKP2 offer new opportunities for targeted ACC therapies.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/metabolismo
Células-Tronco Neoplásicas/metabolismo
Tolerância a Radiação
Receptor Notch1/metabolismo
Fatores de Transcrição SOXE/metabolismo
[Mh] Termos MeSH secundário: Antígeno AC133/genética
Antígeno AC133/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Animais
Biomarcadores Tumorais
Carcinoma Adenoide Cístico/genética
Carcinoma Adenoide Cístico/patologia
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Modelos Animais de Doenças
Proteína 7 de Ligação a Ácidos Graxos/metabolismo
Perfilação da Expressão Gênica
Xenoenxertos
Seres Humanos
Ligantes
Camundongos
Camundongos Nus
Gradação de Tumores
Ligação Proteica
Radiação
Tolerância a Radiação/genética
Receptor Notch1/genética
Proteínas Quinases Associadas a Fase S/metabolismo
Fatores de Transcrição SOXE/genética
Células Tumorais Cultivadas
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers, Tumor); 0 (FABP7 protein, human); 0 (Fatty Acid-Binding Protein 7); 0 (Ligands); 0 (Receptor, Notch1); 0 (S-Phase Kinase-Associated Proteins); 0 (SOX10 protein, human); 0 (SOXE Transcription Factors); 0 (Tumor Suppressor Proteins); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 3.4.- (Amyloid Precursor Protein Secretases)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160417
[St] Status:MEDLINE
[do] DOI:10.1158/1078-0432.CCR-15-2208



página 1 de 140 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde